Abstract
Incubation of guinea-pig cerebral cortical slices with the excitatory amino acid agonists dl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) or N- methyl- d-aspartate (NMDA) failed to significantly alter either basal or 5′- N-ethylcarboxamidoadenosine-(NECA-)stimulated cAMP levels. Quisqualate, l-glutamate and dl-1-aminocyclopentane- trans-1,3-dicarboxylate ( t-ACPD) were also without effect on basal levels of cAMP but increased NECA-stimulated levels of cAMP to approximately 190, 220 and 290% of control levels, respectively. Analysis of t-ACPD concentration-response data for the potentiation of NECA-stimulated cAMP elevations and the stimulation of phosphoinositide turnover gave EC 50 values of 51 and 107 μM, respectively. The enhancing effect of t-ACPD on cAMP levels was maintained for up to 40 minutes as was the stimulation of phosphoinositide turnover. We conclude that the cAMP response to A 2b adenosine receptor stimulation is augmented by the rigid glutamate analogue t-ACPD, possibly through the action of products of phosphoinositide turnover.
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